黑色素通过保留H3K9甲基化和SIRT3来改善PM2.5诱导的精子生成障碍
Jianhui Liu1,2, Moxuan Zhao2, Xiaomin Dong3
1Department of Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital, Beijing, China.
Environmental toxicology
|November 23, 2023
概括
暴露于颗粒物 (PM2.5) 损害了男性的生育能力,因为它扰乱了变和增加了丸细胞的亡. 黑色素治疗可以防止PM2.5诱导的生殖毒性,保持精子质量.
科学领域:
- 环境健康 环境健康
- 生殖生物学 生殖生物学
- 毒理学 毒理学 毒理学
背景情况:
- 空气污染,特别是细颗粒物 (PM2.5),越来越多地与男性不孕症有关.
- 确切的PM2.5影响精子发生的机制和黑激素的潜在保护作用仍然不清楚.
研究的目的:
- 阐明PM2.5暴露如何破坏男性生殖过程,重点是精子生成和半体变异.
- 调查黑能否减轻PM2.5诱导的雄性小鼠的生殖毒性.
主要方法:
- 对ApoE-/-小鼠暴露于PM2.5和测试丸参数的评估.
- 对细胞亡,变相关蛋白质 (γ-H2AX,Stra8) 和表观遗传修饰 (H3K9甲基化,p53脱甲基化) 的分析.
- 评估黑激素对PM2.5引起的损伤的保护作用.
主要成果:
- 暴露于PM2.5抑制了Nrf2抗氧化途径,增加了丸亡,并通过改变关键蛋白质扰乱了化.
- PM2.5破坏了G9a依赖的H3K9甲基化和SIRT3介导的p53脱乙烯化,与精子数量和运动率的降低相关.
- 黑色素治疗有效地保留了H3K9甲基化和SIRT3/p53脱甲基化,缓解了PM2.5诱导的半变异抑制和亡.
结论:
- 暴露于PM2.5会通过G9a/H3K9途径扰乱微分,并通过SIRT3/p53途径诱导亡,从而导致男性不孕.
- 黑色素显示出对PM2.5诱导的男性生殖毒性的保护作用,提供了潜在的治疗见解.
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